Dustin Anderson

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Dustin Anderson PhD/MD Student
DiplT Electronics Engineering Technology BCIT
BSc Simon Fraser University

Hotchkiss Brain Institute
Health Research Innovation Center (HRIC) 1B42A
University of Calgary
Calgary Alberta Canada
T2N 4N1
Phone: 403-220-8451
FAX: 403-210-7446
andersdm@ucalgary.ca

Training
2002
DiplT Electronics Engineering Technol.
BC Institute of Technology
Vancouver Canada

2007 -
BSc Cell Molecular Biology
Simon Fraser University
Vancouver Canada

2007 -
PhD / MD - [In Progress]
University of Calgary
Supervisors: R.W. Turner/G.W. Zamponi

Special Courses 2008 Frontiers in Neurophotonics Laval University
Awards BSc 2005 - SFU Open Scholarship Golden Key Int. Honours Soc.	2006 - John and Isabel Young Bursary - SFU Open Scholarship - SFU Alumni Scholarship	2007 - - SFU Open Scholarship - SFU Alumni Scholarship - Nat. Neurosci. Compet., UofC
PhD - Achievers in Medical Science (AIMS) - Chen Fong Scholarship HBI - Queen Elizabeth II Scholarship	- TA Cellular & Molecular Neuroscience - AIMS Excellence in Research (2) - MDNS Program Specific Award (3) - Dean's Publication and Mentorship Prize 2010
- Leaders in Medicine Program - AHFMR Studentship - I. Walton Killam Scholarship - Silver Medal, CIHR National Research Poster Competition - Governor General 's Gold Medal Award - PhD 2011 - Dept. Neuroscience nominee - CAGS/UMI Distinguished Dissertation Award 2012

Research Focus: The basis of T type ion channel interactions

Approach:

Electrophysiology in vitro, pharmacology, two-photon imaging

Preparations:

In vitro slice preparations, tissue sections

Below are short summaries of projects published from my research.

	Model - Stellate cells Cerebellar stellate cells respond to membrane hyperpolarizations with a non-monotonic first spike latency due to the co-expression of T-type calcium and A-type potassium channels. My project focuses on the interplay between these currents that determine the timing of first spike discharge following membrane hyperpolarizations.

Representative examples of Transient and Weak Burst Cell spike rebounds

Distinct ion channel contributions to burst phenotype in deep cerebellar neurons
The large diameter putative projection neurons of rat deep cerebellar nuclei have been shown to generate either a Transient or Weak rebound Burst phenotype that was linked to the selective expression of T-type calcium channel isoforms. Here we show that the two burst phenotypes also reflect a differential functional availability of LVA T type calcium current at burst threshold, and different contributions of repolarizing potassium currents that shape burst properties. See Molineux et al. (2008). PDF

Synaptically evoked rebound bursts in deep cerebellar neurons
Rebound burst discharge in deep cerebellar nuclear (DCN) cells is readily evoked through direct current injection, but the probability of evoking rebounds with inhibitory synaptic stimulation is less certain. Here we show that stimulation of Purkinje cell inhibitory inputs to DCN neurons in vitro evokes rebound bursts that can be distinguished according to two known phenotypes of burst output. Reliable rebound burst generation indicates the potential for this activity to contribute to cerebellar output in response to physiological activity in vivo. See Tadayonnejad et al. (2009). PDF

KChiP3 mediated shift in Kv4 inactivation

A Cav3-Kv4 signaling complex regulates A type current and neuronal activity
A-type potassium channels of the Kv4 family regulate the latency and frequency of spike output in numerous CNS cells. Kv4 channels complex with Potassium Channel Interacting Proteins (KChIPs), a family of calcium sensor proteins that should confer calcium sensitivity. However, neither the physiological source for calcium nor its effects on A-type current were known. Here we show that T-type (Cav3) calcium channels associate with the Kv4 complex to selectively modulate Kv4 inactivation and establish function in a physiological range. See Anderson et al. (2010).

The Cav3.1 calcium channel modulates Kv4.2 voltage for inactivation
Here we show that the Cav3.1 (T-type) calcium channel isoform also associates with the Kv4.2 complex to selectively right-shift Kv4 inactivation, but to a lesser extent than for other Cav3 channel isoforms. A link between Cav3.1 and Kv4.2 is further indicated through coimmunoprecipitation and pulldowns with Cav3.1 fusion proteins.
See Anderson et al. (2010b), Addendum.

IT and IH have distinct roles in DCN rebound bursts

Distinct roles for IT and IH in controlling deep cerebellar rebound responses
Here we examined the role for IT and IH in generating the rebound responses that are evoked in deep cerebellar neurons in response to inhibitory input from Purkinje cells. We used recordings in vitro and modeling to find that only a small fraction of the total IT and IH available to a cell are activated by physiological levels of hyperpolarization. However, the currents activated are still sufficient to differentially control the latency, frequency and precision of spike firing during the immediate phase of a rebound response. See Engbers et al. (2011).

Peer-reviewed Publications

Molineux, M.L., Mehaffey, W.H., Tadayonnejad, R., Anderson, D., Tennent, A.F. and Turner, R.W. (2008) Ionic factors governing rebound burst phenotype in rat deep cerebellar neurons. J. Neurophysiology 100:2684-2701. PDF

Tadayonnejad, R., Mehaffey, W.H., Anderson, D. and Turner, R.W. (2009) Reliability of triggering postinhibitory rebound bursts in deep cerebellar neurons. Channels 3(3): 149-155. Open Access.

Anderson, D., Mehaffey, W.H., Iftinca, M., Rehak, R., Engbers, J.D.T., Hameed, S., Zamponi, G.W. and Turner, R.W. (2010) Regulation of neuronal activity by Cav3-Kv4 channel signaling complexes. Nature Neuroscience 13: 333-337. Link Faculty of 1000 citation.

Anderson, D., Rehak, R., Hameed, S., Mehaffey, W.H., Zamponi, G.W. and Turner, R.W. (2010) Regulation of the Kv4.2 complex by Cav3.1 channels. Channels 4(3): 163-167. Open Access PDF

Engbers, J.D.T.*, Anderson, D.*, Tadayonnejad, R.*, Mehaffey, W.H., Molineux, M.L. and Turner, R.W. (2011) Distinct roles for IT and IH in controlling the frequency and timing of rebound spike responses. J. Physiol (Lond.), 589 (Pt 22): 5391-413. * Shared first authors.

Engbers, J.D.T.*, Anderson, D.*, Asmara, H., Rehak, R., Mehaffey, W.H., Hameed, S., McKay, B.E., Kruskic, M., Zamponi, G.W. and Turner, R.W. (2011) Intermediate conductance calcium-activated potassium channels modulate summation of parallel fiber input in cerebellar Purkinje cells. PNAS, In Press. * Shared first authors.

Invited Chapters

McKay, B.E., Tadayonnejad, R., Anderson, D., Engbers, J.D.T., Iftinca, M. and Turner, R.W. (2010) Establishing in vivo like activity in rat cerebellar cells maintained in vitro. Isolated Neural Circuits, in Neuromethods (Ballanyi, K., ed.), Springer In Press.

Tadayonnejad, R., Anderson, D., Molineux, M.L., Mehaffey, W.H., Jayasuriya, K. and Turner, R.W. (2011) Rebound discharge in deep cerebellar nuclear neurons in vitro. Cerebellum 9(3): 352-374. PDF

Turner, R.W., Anderson, D. and Zamponi, G.W. (2011) Signaling complexes of voltage gated calcium channels. Channels 5(5): 440-448.

Invited Talks

Department of Neurobiology, Harvard Medical School, Boston MA. The Cav3-Kv4 complex.

Key Abstracts - Published work

Iftinca M, Anderson D., Rehak, R., Molineux, M.L., McRory, J., Zamponi, G.W. and Turner, R.W.   T-type calcium channels provide calcium-dependent modulation of A-type potassium channels. Can. Assoc. Neurosci. Montreal 2008.

Anderson, D., Mehaffey, W.H., Engbers, J.D.T, Rehak, R., Hamid, S., Zamponi, G.W. and Turner, R.W. T-type mediated calcium influx dynamically modulates Kv4 inactivation. Can. Assoc. Neurosci. Vancouver 2009.

Anderson, D., Iftinca, M., Mehaffey, W.H., Rehak, R., Hami,d S., Zamponi, G.W. and Turner, R.W. A-type potassium channels are dynamically regulated by T-type calcium current. IUPS Kyoto 2009.

Turner, R.W., Anderson, D., Iftinca, M., Mehaffey, W.H., Rehak, R., Hamid, S., Zamponi, G.W. Regulation of neuronal activity by Cav3-Kv4 channel signaling complexes. Ion Channels & Transporters Mtg, Lake Biwa, Kyoto Japan, 2009.

Anderson, D., Iftinca, M., Mehaffey, W.H., Rehak, R., Engbers, J.D.T., Hamid, S., Zamponi, G.W. and Turner, R.W. Regulation of neuronal output by Cav3-Kv4 signalling complexes. Proc. Soc. Neurosci. 2009.

Tadayonnejad, R., Engbers, J.D.T., Anderson, D., Mehaffey, W.H. and Turner, R.W. The role of IH and IT in controlling rebound burst properties of Deep Cerebellar Nuclear cells. Can Assoc. Neurosci., 2010.

Tadayonnejad, R., Engbers, J.D.T., Anderson, D., Mehaffey, W.H. and Turner, R.W. IT and IH selectively regulate rate coding and spike precision in deep cerebellar nuclear cells. Proc. Soc. Neurosci., 2010.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Zamponi, G.W. and Turner, R.W.   T-type/IK channel signalling complex modulates summation of parallel fiber inputs in cerebellar Purkinje cells. Can. Assoc. Neurosci. 2010.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Zamponi, G.W. and Turner, R.W.   IKCa channels establish a high pass filter for parallel fiber input in cerebellar Purkinje cells. Gordon Conference, Cerebellum in Health and Disease, New London, NH, 2011.

Engbers, J.D.T., Anderson, D., Rehak, R., Asmara, H., Mehaffey, W.H., Hameed, S., McKay, B.E., Kruskic, M., Zamponi, G.W., Turner, R.W. IKCa-Cav3 complex reduces temporal summation of parallel fiber input in cerebellar Purkinje cells. IBRO World Congress of Neuroscience, Florence, Italy, 2011.

Engbers, J.D.T., Anderson, D., Rehak, R., Mehaffey, W.H., McKay, B.E., Kruskic, M., Zamponi, G.W., Turner, R.W. IKCa-Cav3 complex creates a high pass filter for parallel fiber input in cerebellar Purkinje cells. Comp. Neurosci., Stockholm, Sweden, 2011. Prize, Student Poster Presentation.